Professional Documents
Culture Documents
Disorders
By,
Aswathy Krishnan,
1st Yr
M Sc. Nursing(2008-2010)
Bombay Hospital College of Nursing
GI System – Structure & Functions
Propulsion
Peristaltic contractions
Digestion
Mixing
Enzymatic breakdown
Absorption of nutrients
Defecation
GI System - Anatomy
Mouth
Anterioly bounded by lips
Posteriorly bounded by the
oropharynx
Mechanical and chemical
digestion (secretion of saliva by
salivary glands)
Stomach
Fundus (top) body pylorus
Pyloric sphincter
Mechanical and chemical
digestion: Mixing food and acid
and enzymes to create chyme.
Goblet Cells
Parietal Cells
Chief Cells
G Cells
Blood supply : Celiac artery
Venous drainage in to portal vein
GI System - Anatomy
Small intestine
~ 5m (~16.7’) tube
From Pyloris to Ileocecal Valve
Duodenum jejunum
ileum
Circular folds and villae to
increase surface area
Most digestion and absorption
takes place here via intestinal
enzymes and exocrine
secretions from the liver and
pancreas (which enter the
duodenum via ducts)
Liver
Located in the upper rt. Abdomen
Rt, Lt.& caudate lobes ,subdivided into segments
Blood supply: Portal Vein, Hepatic Artery
Roles of the liver:
Conjugation of billurubin
Synthesis and deactivation of clotting factors
Phagocytosis
Detoxification
Processes nutrients
Gallbladder
Sac like organ attached to Liver
Storage facility for bile(50ml.)
CCK stimulates contraction of Gall bladder
Bile composition: water, bile salts (emulsify lipids), bile pigments]
Blood Supply: Cystic & hepatic artery
Biliary Ducts
Ducts of the Billiary tract very imp in proper functioning of GIS
Bile Calculli Left, Right Hepatic duct Common hepatic duct
Cystic Duct + Common hepatic duct Common Bile Duct duodenum
Accessory organs: pancreas and liver
Pancreas
Endocrine Functions
Production of Insulin, glucagon, somatostatin
Exocrine Function
Pancreatic enzymes: Trypsin, lipase and amylase
Bicarbonate: help neutralize the acidity of the chyme
Blood Supply: Hepatic and cystic artery
Health Assessment- History Taking
Dietary habits
The number of meals ate per day.
Meal times.
Food restrictions or special diets followed.
Changes in appetite. Increased? Decreased? No appetite?
What foods, if any, have been eliminated from the diet? Why?
What foods are not well tolerated?
Alterations in taste.
Personal Habits
Use of Tobacco, alcohol
Past History
Previous GI disease?
Past treatment and surgery?
Medications used. Dosage and frequency
Bowel patterns
Frequency of bowel movements.
Use of laxatives and/or enemas.
Changes in bowel habits.
Stool Description.
(a) Constipation.
(b) Diarrhoea.
(c) Blood in stool.
(d) Mucous in stool.
(e) Black, tarry stools.
(f) Pale or clay colored stools.
(g) Foul smelling stools.
(h) Pain with stool
Abdominal Pain
Location? Frequency? Duration? Character of the pain? Pattern? distribution
of reffered pain & associated factors
Indigestion
Frequency? Duration? Associated with specific foods? Relieved by?
Gas (belching and flatus).
Frequency? Associated with specific foods? Relieved by?
Nausea, Vomiting
Frequency? Duration? Associated with meals? Character of emesis?
Relieved by?
Health Assessment- Physical
Perform a brief, general head-to-toe visual inspection of the
patient. Are height and weight within normal range for the
patient's age and body type
Observe the skin for Color (pale, jaundiced), Surgery scars,
Bruises, Rashes, Lesions, Turgor and moisture content,
Edema.
Examine the mouth and throat.
Look at the lips, tongue, and mucous membranes, noting
abnormalities such as cuts, sores, or discoloration.
Observe the condition of the teeth..
Observe the gums. Are they healthy and pink? Examination
of the abdomen
Physical examination of the abdomen involves visual
inspection, auscultation, and palpation
patient is resting in a supine position, knees slightly flexed
to relax the abdominal muscles
abdomen is viewed as four quadrants
AUSCULTATION
• Ausculate all four quadrants
•Listen for bowel sounds. The best location is
below and to the right of the umbilicus.
• Describe the sounds heard according to
location, frequency, and character of the sound.
• Abnormalities include absent bowel sounds
and the peristaltic rush of a hyperactive bowel.
PALPATION
• Palpate all four quadrants
•used to detect muscle guarding, tenderness,
and masses.
• Record Rigidity or Guarding, Pain or
Tenderness, Rebound Pain Masses.
Diagnostics
Laboratory Tests
Blood Test
Complete blood count RBC, Hb, HCT
Electrolytes
Sodium, Pottasium
CEA : Blood tumor marker
Colon cancer
Serum enzymes
amylase, lipase, alkaline phosphatase, SGOT, SGPT, and LDH
Check liver function
Eval serum protein levels, clotting times, serum liver enzymes, bilirubin levels
Pancreatic function
Serum enzyme levels
Faecal Analysis
occult blood, lipids, urobilinogen, ova, parasites, and other substances
consider the patient's diet when assessing and documenting the character of a
patient's stool.
Gastric analysis
presence, amount, or absence of hydrochloric acid
presence of cancer cells
types and amounts of enzymes present.
Abdominal Ultrasonography
Radiographic Test
upper GI Series ( Barium swallow)
normally held NPO
gum chewing, smoking discouraged as it stimulates gastric action.
Lower GI Series ( Barium Enema)
patient is held NPO
Constipation a side effect of the contrast medium
Endoscopy
Upper GI endoscopy
Upper Gastrointestanal Fibroscopy/ Esophagogastrodeodenoscopy
patient must be fasting
Lower GI endoscopy
proctoscopy, sigmoidoscopy and colonoscopy
Bowel should be free of stool to enhance visualization
Endoscopy through Ostomy
Laproscopy
Pathophysiology
Gastroesophageal reflux results from transient relaxation or
incompetence of lower esophageal sphincter, or increased
pressure within stomach
Prolonged reflux –oesophigitis
Clinical Manifestations
Heartburn, dysphagia.
Diagnostic Tests
Barium swallow (evaluation of esophagus, stomach, small
intestine)
Upper endoscopy: direct visualization; biopsies may be done
Esophageal manometry, which measure pressures of esophageal
sphincter and peristalsis
Esophageal motility studies
Medications
Antacids for mild to moderate symptoms
H2-receptor blockers: decrease acid production; given BID or more
often, e.g. cimetidine, ranitidine, famotidine, nizatidine
Proton-pump inhibitors: reduce gastric secretions, promote healing
of esophageal erosion and relieve symptoms, e.g. omeprazole;
lansoprazole initially for 8 weeks; or 3 to 6 months
Promotility agent: enhances esophageal clearance and gastric
emptying, e.g. metoclopramide
Gastroesophageal Reflux Disease
(GERD)
Dietary and Lifestyle Management
Elimination of acid foods (tomatoes, spicy, citrus foods,
coffee
Avoiding food which relax esophageal sphincter or delay
gastric emptying (fatty foods, chocolate, alcohol)
Eat small meals and stay upright 2 hours post eating; no
eating 3 hours prior to going to bed
Elevate head of bed to decrease reflux
No smoking
Surgical Management
Laparoscopic procedures to tighten lower esophageal
sphincter
Open surgical procedure: Nissen fundoplication - upper
portion of the stomach is wrapped around the distal
oesophagus and sutured, creating a tight LES
Nursing Care
Pain usually controlled by treatment
Assist client to institute home plan
Complications
Esophageal stricture , ulceration
of the esophagus, Barrett’s
oesophagus
Hiatal Hernia
A condition in which cardiac sphincter becomes enlarged
allowing the stomach to pass in to the thoracic cavity
Sliding hernia
More common
Predisposing factors
Increased intra-abdominal pressure
Increased age
Trauma
Congenital weakness
Manifestations
Heartburn
Brief substernal burning sensation
Freq belching
Discomfort when lying supine
Diagnostic Tests
Barium swallow
Endoscopy
Treatment
Similar to GERD
NSG Management
Gastritis
Inflammation of stomach lining from irritation of gastric mucosa
(normally protected from gastric acid and enzymes by mucosal
barrier)
Acute Gastritis
Disruption of mucosal barrier allowing hydrochloric acid and pepsin
to have contact with gastric tissue: leads to irritation, inflammation,
superficial erosions
Gastric mucosa rapidly regenerates; self-limiting disorder
Causes of acute gastritis
Irritants include aspirin and other NSAIDS, alcohol, caffeine
Ingestion of corrosive substances: alkali or acid
Effects from radiation therapy, certain chemotherapeutic agents
Erosive Gastritis: form of acute which is stress-induced, complication
of life-threatening condition (Curling’s ulcer with burns); gastric
mucosa becomes ischemic and tissue is then injured by acid of
stomach
Manifestations
Mild: anorexia, mild epigastric discomfort, belching
More severe: abdominal pain, nausea, vomiting, hematemesis,
melena
Diaehoea, the contaminated food is the cause of gastritis
Treatment
NPO status to rest GI tract for 6 – 12 hours, reintroduce clear liquids
gradually and progress; intravenous fluid and electrolytes if indicated
Medications: proton-pump inhibitor or H2-receptor blocker; sucralfate
acts locally; coats and protects gastric mucosa
If gastritis from corrosive substance: immediate dilution and removal
of substance by gastric lavage (washing out stomach contents via
nasogastric tube), no vomiting
Gastritis - Chronic
Superficial Gastritis
Atrophic Gastritis
Type A: Parietal cells normally secrete intrinsic factor
needed for absorption of B12, when they are destroyed by
gastritis pts develop pernicious anemia
Type B: more common and occurs with aging; caused by
chronic infection of mucosa by Helicobacter pylori; associated
with risk of peptic ulcer disease and gastric cancer
Hypertrophic Gastritis
Manifestations
Vague gastric distress, epigastric heaviness not relieved by
antacids
Fatigue associated with anemia; symptoms associated with
pernicious anemia
Treatment
Type B: eradicate H. pylori infection with combination therapy
of two antibiotics (metronidazole (Flagyl) and clarithomycin or
tetracycline) and proton–pump inhibitor (Prevacid or Prilosec)
Bland Diet
Small Frequent meals
Antacids
Administer vitamin B12
Diagnostic Tests
Gastric analysis: assess hydrochloric acid secretion (less with
chronic gastritis)
Hemoglobin, hematocrit, red blood cell indices: anemia
including pernicious or iron deficiency
Serum vitamin B12 levels: determine pernicious anemia
Upper endoscopy: visualize mucosa, identify areas of bleeding,
obtain biopsies; may treat areas of bleeding with electro or laser
coagulation or sclerosing agent
Peptic Ulcer Disease (PUD)
refers to ulcerrations in the mucosa of the lower oesophagus , stomachor dueodenum
Incidence
Duodenal ulcers: most common; affect mostly males ages 30 – 55; ulcers found near
pyloris
Gastric ulcers: affect older persons (ages 55 – 70); found on lesser curvature and
associated with increased incidence of gastric cancer
Pathophysiology
ACTH & Cortisone
Structure of mucosa
Amount of Mucous produced
Trauma, infection, physical or psychological stress can cause increase in gastric
secretion, blood supply and gastric motility by way of thalamus stimulus to vagal nerve
Use of NSAIDS: interrupts prostaglandin synthesis which maintains mucous barrier of
gastric mucosa
Types
Duodenal Ulcers
Ususlly occur 1.5 cm. from pylorus
Hypersecretion of acid
Protien rich meals, Calcium, vagal stimulation
Gastric ulcers
Junction of fundus and pylorus
Caused by break in mucosal barrier due to incompetent pylorus
Peptic Ulcer Disease (PUD)
Manifestations
Pain: gnawing, burning, aching, cramplike
Gastric
when stomach is full and relieved by vomiting
Upper epigastric region
Duodenal
when stomach is empty and relieved by food
Left epigastric region
Nausea and vomiting
generally associated with Gastric ulcers
Treatment
Rest and stress reduction
Nutritional management
Pharmacological management
Antacids (Mylanta)
Neutralizes acids
Proton pump inhibitors (Prilosec, Prevacid)
Block gastric acid secretion
Histamine blockers (Tagamet, Zantac, Axid)
Blocks gastric acid secretion
Carafate
Forms protective layer over the site
Mucosal barrier enhancers (colloidal bismuth, prostoglandins)
Protect mucosa from injury
Antibiotics (Amoxicillin, Ampicillin)
Treat H. Pylori infection
Surgical intervention
Minimally invasive gastrectomy
Partial gastric removal with laproscopic surgery
Bilroth I and II
Removal of portions of the stomach
Vagotomy
Cutting of the vagus nerve to decrease acid secretion
Pyloroplasty
Widens the pyloric sphincter
Nursing Management
Administer medication as ordered
Client Teaching & discharge plan
Medical regimen
Diet
Avoidance of stress producing situations
Complications
Hemorrhage: frequent in older adults
Gastric outlet (pyloric sphincter) obstruction: edema surrounding ulcer blocks GI tract
from muscle spasm or scar tissue
Perforation: ulcer erodes through mucosal wall and gastric or duodenal contents enter
peritoneum leading to peritonitis; chemical at first (inflammatory) and then bacterial in 6
to 12 hours
Cancer of Stomach
Malignant neoplasms found in the stomach,usually Adenocarcinoma
Etiology and risk factors
Presence of H pylorai inf. in the stomach
Chronic atrophic gastritis, adenomatous polyps, pernicious anemia
Increase in absorption of carcinogens from diet
Genetic factors
Pathophysiology
Adenocarcinoma most common form involving mucus-producing cells
of stomach in distal portion
Begins as localized lesion (in situ) progresses to mucosa; spreads to
lymph nodes and metastasizes early in disease to liver, lungs, ovaries,
peritoneum
Manifestations
Disease often advanced with metastasis when diagnosed
Early symptoms are vague: early satiety, anorexia, indigestion,
vomiting, pain after meals not responding to antacids
Later symptoms weight loss, cachexia (wasted away appearance),
abdominal mass, stool positive for occult blood
Presence of lactic acid and LDH
Diagnostic tests
Upper GI tract X ray exam
Upper endoscopy: visualization and tissue biopsy of lesion
Medical Management
Client may receive Chemotherapy or radiation therapy
Primary treatment is surgical management
Surgery, if diagnosis made prior to metastasis
Partial gastrectomy with anastomosis to duodenum: Bilroth I or gastroduodenostomy
Partial gastrectomy with anastomosis to jejunum: Bilroth II or gastrojejunostomy
Total gastrectomy (if cancer diffuse but limited to stomach) with esophagojejunostomy
Appendicitis
It is an inflammation of the vermiform
appendix that develops most
commonly in adolescents and young
adults
Etiology
A fecalith which occludes the lumen of
appendix
Kinking
Swelling of the bowel wall
External occlusion of the bowel
Pathophysiology
Appendix obstructed > intrlumunar
pressure increases > Venus drainage
decreases > thrombosis, edema bacterial
infection > hyperaemia of appendix
Manifestations
Surgical Management
Complictions
Perforation of the bowel
Colon Cancer
Pathophysiology
Most malignancies begin as adenomatous polyps and arise in rectum and
sigmoid
Spread by direct extension to involve entire bowel circumference and
adjacent organs
Metastasize to regional lymph nodes via lymphatic and circulatory systems
to liver, lungs, brain, bones, and kidneys
Manifestations
Often produces no symptoms until it is advanced
Presenting manifestation is bleeding; also change in bowel habits (diarrhea
or constipation); pain, anorexia, weight loss, palpable abdominal or rectal
mass; anemia
Complications
Bowel obstruction
Perforation of bowel by tumor, peritonitis
Direct extension of cancer to adjacent organs; reoccurrences within 4 years
Diagnostic Tests
CBC: anemia from blood loss, tumor growth
Fecal occult blood (guiac or Hemoccult testing): all colorectal cancers bleed
intermittently
Carcinoembryonic antigen (CEA): not used as screening test, but is a tumor
marker and used to estimate prognosis, monitor treatment, detect
reoccurrence may be elevated in 70% of people with CRC
Colonoscopy or sigmoidoscopy; tissue biopsy of suspicious lesions, polyps
Chest xray, CTscans, MRI, ultrasounds: to determine tumor depth, organ
involvement, metastasis
Pre-op care
Consult with ET nurse if ostomy is planned
Bowel prep with GoLytely
NPO
NG
Surgery
Surgical resection of tumor, adjacent colon, and regional lymph nodes is
treatment of choice
Whenever possible anal sphincter is preserved and colostomy avoided;
anastomosis of remaining bowel is performed
Tumors of rectum are treated with abdominoperineal resection (A-P
resection) in which sigmoid colon, rectum, and anus are removed through
abdominal and perineal incisions and permanent colostomy created
Colostomy
Ostomy made in colon if obstruction from tumor
Temporary measure to promote healing of anastomoses
Permanent means for fecal evacuation if distal colon and rectum removed
Named for area of colon is which formed
Sigmoid colostomy: used with A-P resection formed on LLQ
Double-barrel colostomy: 2 stomas: proximal for feces diversion; distal is mucous
fistula
Transverse loop colostomy: emergency procedure; loop suspended over a bridge;
temporary
Hartman procedure: Distal portion is left in place and oversewn; only proximal
colostomy is brought to abdomen as stoma; temporary; colon reconnected at later
time when client ready for surgical repair
Post-op care
Pain
NG tube
Wound management
Stoma
Should be pink and moist
Drk red or black indicates ischemic necrosis
Look for excessive bleeding
Observe for possible separation of suture securing stoma to abdominal wall
Evaluate stool after 2-4 days postop
Ascending stoma (right side)
Liquid stool
Transverse stoma
Pasty
Descending stoma
Normal, solid stool
Radiation Therapy
Used as adjunct with surgery; rectal cancer has high rate of regional recurrence if tumor
outside bowel wall or in regional lymph nodes
Used preoperatively to shrink tumor
Provides local control of disease, does not improve survival rates
Chemotherapy:
Used postoperatively with radiation therapy to reduce rate of rectal tumor recurrence and
prolong survival
Nursing Care
Prevention is primary issue
Client teaching
Diet: decrease amount of fat, refined sugar, red meat; increase amount of fiber; diet
high in fruits and vegetables, whole grains, legumes
Screening recommendations
Seek medical attention for bleeding and warning signs of cancer
Risk may be lowered by aspirin or NSAID use
Nursing Diagnoses for post-operative colorectal client
Pain
Imbalanced Nutrition: Less than body requirements
Anticipatory Grieving
Alteration in Body Image
Risk for Sexual Dysfunction